Patients with intractable malignant pain do not now have available a generally satisfactory means of pain control. Narcotics cloud the sensorium, and tolerance develops rapidly. Surgery for pain relief may be hazardous, and often results in loss of muscle tone and weakness. A promising alternative is analgesia by electrical neurostimulation. The effect has been well demonstrated in clinical studies, but little is known of the mechanisms underlying this form of analgesia. The "gate control" theory of pain, which gave rise to the application of the method, proposes that stimulation of large sensory fibers "closes the gate" to incoming pain signals in the dorsal horn of the spinal cord. However, clinical experience and preliminary studies suggest a "fatigue" of small pain fibers as an alternative hypothesis. We propose a series of studies to examine the mechanisms of electrical analgesia and to test the two differing hypotheses: (1) quantitative neurological sensory examination of patients who use transcutaneous neurostimulators for relief of benign pain, to determine the nature and extent of sensory changes caused by electrical stimulation; (2) measurement of cortical evoked potentials in patients who use transcutaneous neurostimulators; (3) studies of peripheral nerve evoked potentials in animals with and without neurostimulation; and (4) studies of axoplasmic transport in peripheral nerve following electrical stimulation. These experiments will permit an explanation of peripheral electrical analgesic mechanisms, perhaps modifying our theories of pain control, and permitting the development of a more effective application of the technique to patients with intractable malignant pain.